Abstract
For myocarditis and inflammatory cardiomyopathy, an etiologically driven treatment is today the best option beyond heart failure therapy. Prerequisites for this are noninvasive and invasive biomarkers including endomyocardial biopsy and polymerase chain reaction on cardiotropic agents. Imaging by Doppler echocardiography and cardiac magnetic resonance imaging as well as cardiac biomarkers such as C‑reactive protein, N‑terminal pro-B-type natriuretic peptide , and troponins can contribute to the clinical work-up of the syndrome but not toward elucidating the underlying cause or pathogenetic process. This review summarizes the phases and clinical features of myocarditis and gives an up-to-date short overview of the current treatment options starting with heart failure and antiarrhythmic therapy. Although inflammation in myocardial disease can resolve spontaneously, often specific treatment directed against the causative agent is required. For fulminant, acute, and chronic autoreactive myocarditis, immunosuppressive treatment has proven to be beneficial in the TIMIC and ESETCID trials; for viral cardiomyopathy and myocarditis, intravenous immunoglobulin IgG subtype and polyvalent intravenous immunoglobulins IgG, IgA, and IgM can frequently resolve inflammation. However, despite the elimination of inflammation, the eradication of parvovirus B19 and human herpesvirus-6 is still a challenge, for which ivIg treatment can become a future key player.
Highlights
Infectious myocarditis0.02 IGRA (Quantiferon) or microscopy from sputum, pericardial fluid, in Africa more frequent
In patients with dilated cardiomyopathy with or without inflammation, antibradycardia pacing in second- and third-degree atrioventricular block or in bradyarrhythmia is well established
This review summarizes the phases and clinical features of myocarditis and gives an up-to-date short overview of the current treatment options starting with heart failure and antiarrhythmic therapy
Summary
0.02 IGRA (Quantiferon) or microscopy from sputum, pericardial fluid, in Africa more frequent. Viral infection, according to common belief, may trigger an autoreactive cellular and humoral immune response that leads to myocardial damage with inflammation. Following this pathogenetic hypothesis, immunosuppressive treatment either by prednisone alone or in combination with azathioprine or cyclosporine was examined in five trials, the results of which are summarized in. The Myocarditis Treatment Trial (MTT) by Mason et al in 1995 [22] showed neither a benefit nor an increased mortality after a 6-month treatment with cyclosporine A or azathioprine and prednisone when compared with placebo. Wojnicz et al randomized 84 patients with dilated heart muscle disease and increased human leukocyte antigen (HLA) expression for a treatment of azathioprine and prednisone or placebo for 3 months. The ESETCID (European Study on the Epidemiology and Treatment of Cardiac Inflammatory Disease) is a doubleblind, randomized, placebo-controlled three-armed trial with prednisolone and azathioprine for autoreactive (virus negative) inflammatory dilated cardiomy-
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